Herpes simplex virus (HSV) is a commonly used reference to two members of the Herpesviridae family, herpes simplex virus 1 (HSV-1) and herpes simplex virus 2 (HSV-2). An active HSV-1 infection causes mainly oral herpes, which may result in small blisters around face or mouth. An active HSV-2 infection generally affects the genital area, causing blisters that can break open and result in small ulcers. Tingling or shooting pains may occur before the blisters appear. Worldwide, about 90% of people are infected with one or both of HSV-1 and HSV-2 with HSV-1 infection much more prevalent than HSV-2 infection. About 65% of persons in the United States have antibodies to HSV-1 and about 16% of Americans between the ages of 14 and 49 are infected with HSV-2.
HSV-1 and 2 have the ability to lie dormant within a cell indefinitely in a latent infection and not be fully eradicated even after treatment. The result is that the virus can reactivate and begin producing large amounts of viral progeny without the host being infected by any new outside virus. In the latent state, the viral genome persists within the host cells as episomes; stabilized and floating in the cytoplasm or nucleus.
There is no cure for HSV and, once infected, a host carries the herpes virus indefinitely, even when not expressing symptoms in an active infection or outbreak. While various antiviral treatments are available, they generally are directed to interrupting the replicating cycle of the virus and, therefore, prove ineffective at eradicating latent infections. Because latent infections can evade immune surveillance and reactivate the lytic cycle at any time, there is a persistent risk to an infected individual of outbreak and the pain and suffering associated with it. The majority of antiviral drug development has been focused on protein targets but such approaches have not been successful in eradicating HSV.